Role of Toll-like receptor 2/4-nuclear factor-κB signaling pathway in invasion of Mycobacterium tuberculosis to mouse dendritic cells.
- Author:
Qian XU
1
;
Meng-mei JIN
1
;
Wen-wen ZHENG
1
;
Li ZHU
1
;
Shui-ling XU
1
Author Information
- Publication Type:Journal Article
- MeSH: Animals; B7-1 Antigen; metabolism; B7-2 Antigen; metabolism; Cells, Cultured; Dendritic Cells; immunology; metabolism; Mice; Mycobacterium tuberculosis; NF-kappa B; metabolism; Signal Transduction; Toll-Like Receptor 2; metabolism; Toll-Like Receptor 4; metabolism; Tumor Necrosis Factor-alpha; metabolism
- From: Journal of Zhejiang University. Medical sciences 2014;43(2):200-206
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanism of Mycobacterium tuberculosis invasion to mouse dendritic cells (DC).
METHODSMycobacterium tuberculosis strain H37Rv was co-cultured with mouse DC2.4 cells.The mRNA expression of Toll-like receptor 2/4(TLR2/4) in DC2.4 cells was detected by fluorescent quantitative real-time PCR and the protein expression of nuclear factor κB(NF-κB) was assessed by Western blotting.The extracellular concentration of tumor necrosis factor α(TNF-α) was measured by ELISA methods during Mycobacterium Tuberculosis invasion.Indirect immunofluorescent staining and flow cytometry assay were used to detect the expression of CD80 and CD86 on DC2.4 cells before and after invasion.
RESULTSThe invasion of Mycobacterium tuberculosis in DC2.4 cells was observed after 2 h of co-incubation.The rates of invasion were (37.9±5.6)%,(51.2±7.6)%,(57.2±8.9)% and(63.9±6.8)% at 6,8,10 and 12 h after co-incubation,respectively.The mRNA expression level of TLR2 /4 was significantly increased at 6 h but decreased at 10 h after co-incubation.The expressions of NF-κB p65 and TNF-α were higher in DC2.4 cells after being invaded by 6,8,and 10 h and then gradually decreased.CD80 and CD86 expression were increased on DC2.4 at 6 h after co-incubation.
CONCLUSIONInvasion of Mycobacterium tuberculosis strain H37Rv to DC might enhance its antigen-presenting function through activation of TLR2/4-NF-kB signaling pathway.
